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IL-13 decreases suceptibility to airway epithelial SARS-CoV-2 infection but increases disease severity in vivo [Bulk RNA-seq]

ABSTRACT: IL-13 decreases suceptibility to airway epithelial SARS-CoV-2 infection but increases disease severity in vivo [Bulk RNA-seq]

PROVIDER: PRJNA1048482 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27046366_1.fastq.gz	Fastqsanger.gz
	SRR27046366_2.fastq.gz	Fastqsanger.gz
	SRR27046367_1.fastq.gz	Fastqsanger.gz
	SRR27046367_2.fastq.gz	Fastqsanger.gz
	SRR27046368_1.fastq.gz	Fastqsanger.gz

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IL-13 decreases suceptibility to airway epithelial SARS-CoV-2 infection but increases disease severity in vivo

Project description:IL-13 decreases suceptibility to airway epithelial SARS-CoV-2 infection but increases disease severity in vivo

| PRJNA1048487 | ENA

IL-13 decreases suceptibility to airway epithelial SARS-CoV-2 infection but increases disease severity in vivo [Bulk RNA-seq]

Project description:Human airway epithelia (HAE) undergo inflammation-induced remodeling in chronic lung diseases such as asthma and chronic bronchitis. The role of type 2 inflammation-induced epithelial remodeling in SARS-CoV-2 infection and the course of COVID-19 is unclear, moreover, there is discrepancy in the literature regarding the potential benefit of treatments that modulate type 2 inflammation. We investigated the role of IL-13-induced inflammation on SARS-CoV-2 binding/entry, replication, and host response in primary HAE cells in vitro and in a model of mouse-adapted SARS-CoV-2 in vivo. IL-13 protected airway epithelial cells from SARS-CoV-2 infection in vitro by decreasing the abundance of ACE2- expressing ciliated cells rather than by neutralization in the airway surface liquid or by interferon-mediated antiviral effects. In contrast, IL-13 worsened the severity of disease in mice in vivo; the effects were mediated by eicosanoid signaling and were abolished in mice deficient in the phospholipase A2 enzyme PLA2G2D. We conclude that IL-13-induced inflammation affects multiple steps of SARS-CoV-2-induced disease pathogenesis. Whereas IL-13-induced inflammation may be protective against initial infection at the airway epithelium, it enhances disease severity once infection progresses in vivo; blockade of IL-13 and/or eicosanoid signaling may be protective against progression to severe lung disease.

2024-06-26 | GSE249304 | GEO

IL-13 decreases susceptibility to airway epithelial SARS-CoV-2 infection but increases disease severity in vivo.

Project description:Treatments available to prevent progression of virus-induced lung diseases, including coronavirus disease 2019 (COVID-19) are of limited benefit once respiratory failure occurs. The efficacy of approved and emerging cytokine signaling-modulating antibodies is variable and is affected by disease course and patient-specific inflammation patterns. Therefore, understanding the role of inflammation on the viral infectious cycle is critical for effective use of cytokine-modulating agents. We investigated the role of the type 2 cytokine IL-13 on SARS-CoV-2 binding/entry, replication, and host response in primary HAE cells in vitro and in a model of mouse-adapted SARS-CoV-2 infection in vivo. IL-13 protected airway epithelial cells from SARS-CoV-2 infection in vitro by decreasing the abundance of ACE2-expressing ciliated cells rather than by neutralization in the airway surface liquid or by interferon-mediated antiviral effects. In contrast, IL-13 worsened disease severity in mice; the effects were mediated by eicosanoid signaling and were abolished in mice deficient in the phospholipase A2 enzyme PLA2G2D. We conclude that IL-13-induced inflammation differentially affects multiple steps of COVID-19 pathogenesis. IL-13-induced inflammation may be protective against initial SARS-CoV-2 airway epithelial infection; however, it enhances disease progression in vivo. Blockade of IL-13 and/or eicosanoid signaling may be protective against progression to severe respiratory virus-induced lung disease.

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IL-13 decreases suceptibility to airway epithelial SARS-CoV-2 infection but increases disease severity in vivo

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-06-28 | GSE249308 | GEO

Gene Expression Effects of IL-13 on Primary Human Airway Epithelial Cells

Project description:Primary culture airway epithelial cells, grown under physiologic air-liquid interface conditions, with, or without IL-13 in order to study the effects of this cytokine on mucous cell metaplasia, an important feature of asthma and COPD. Keywords: IL13, mucus, goblet cell RNA was isolated from primary culture airway epithelial cells grown at air-liquid interface, treated with or without IL-13 for 21 days.

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IL-13 neutralization effect on COVID-19 severity

Project description:IL-13 neutralization effect on COVID-19 severity

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Effect of IL-13 on transcriptome of differentiated human airway mucociliary epithelium

Project description:We used microarrays to detail the global programme of gene expression that occurs in response to treatment of IL-13 on fully-differentiated human airway mucociliary epithelium

2019-01-10 | GSE110799 | GEO

Airborne particulate matter from goat farm increases acute allergic airway responses in mice increases acute allergic airway responses in mice

Project description:Airborne particulate matter from goat farm increases acute allergic airway responses in mice increases acute allergic airway responses in mice

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RNA sequencing of healthy human airway epithelia with IL-13 treatment time course

Project description:The goal of this study was to examine changes to gene expression induced by IL-13 treatment of air-liquid interface cultures of healthy primary human airway epithelia over time.

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Gene Expression Effects of IL-13 on Primary Human Airway Epithelial Cells

2012-12-04 | GSE37693 | GEO